Evidence map›Paper›PMID 31379881›Full record

ArticleFrontiers in immunology2019

Elevated Neuropeptide Y in Endothelial Dysfunction Promotes Macrophage Infiltration and Smooth Muscle Foam Cell Formation.

Bongkun Choi, Min-Kyung Shin, Eun-Young Kim, Ji-Eun Park, Halim Lee, Seong Who Kim, Jae-Kwan Song, Eun-Ju Chang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.4field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 29 citations in OpenAlex.

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  15. The Role of Neuropeptide Y in the Nucleus Accumbens.International journal of molecular sciences · 2021
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Bongkun ChoiDepartment of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea.
Min-Kyung ShinDepartment of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea.
Eun-Young KimDepartment of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea.
Ji-Eun ParkDepartment of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea.
Halim LeeDepartment of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea.
Seong Who KimStem Cell Immunomodulation Research Center, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea.
Jae-Kwan SongDivision of Cardiology, Asan Medical Center, Research Institute for Valvular Heart Disease University of Ulsan College of Medicine, Seoul, South Korea.
Eun-Ju ChangDepartment of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea.
Ulsan College · KRUniversity of Ulsan · KRAsan Medical Center · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial dysfunction has been linked to vascular inflammation and foam cell formation but the underlying mechanisms still remain unclear. We sought to define the factors inducing inflammation and smooth muscle foam cell formation under endothelial dysfunction using endothelial nitric oxide synthase (eNOS)-deficient mice. Vascular smooth muscle cells (VSMCs) from eNOS-deficient mice displayed increased expression of macrophage-related genes and elevated lipid uptake. Neuropeptide Y (NPY) was upregulated in the aorta from the eNOS-deficient mice and promoted macrophage chemotaxis toward VSMCs while enhancing the activity of matrix metalloproteinase-3. Notably, NPY induced lipid uptake in VSMCs, facilitating smooth muscle foam cell formation, in association with enhanced expression of genes related to modified low-density lipoprotein uptake and macrophages. NPY was augmented by inflammatory pentraxin 3 (PTX3) in VSMCs. PTX3 enhanced macrophage migratory capacity through the NPY/neuropeptide Y receptor axis and this effect was attenuated by pharmacological inhibition with a receptor-specific antagonist. These observations suggest that endothelial dysfunction leads to the elevation of NPY that amplifies vascular inflammation by increasing inflammatory cell chemotaxis and triggers smooth muscle foam cell formation.

Indexed as

AnimalsAtherosclerosisChemotaxis, LeukocyteC-Reactive ProteinEndothelium, VascularFoam CellsMacrophagesMiceMice, KnockoutMuscle, Smooth, VascularMyocytes, Smooth MuscleNerve Tissue ProteinsNeuropeptide YNitric Oxide Synthase Type IIIPentraxinsPlaque, AtheroscleroticC-Reactive ProteinNerve Tissue ProteinsNeuropeptide YNitric Oxide Synthase Type IIIPentraxinsendothelial nitric oxide synthase (eNOS)lipidmacrophageneuropeptide Y (NPY)pentraxin 3 (PTX3)smooth muscle foam cell

Identifiers

PMID31379881
PMCPMC6657015
OpenAlexW2958218291

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.